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Table 1 Individual chromosomal islands of up- or down-regulation.

From: A genome-wide map of aberrantly expressed chromosomal islands in colorectal cancer

expression change

start region

end region

start gene

end gene

potential tumor genes, hereditary CRC, known chromosomal imbalances

loss

1p36.33

1p36.32

TNFRSF18

ARHGEF16

amplification of 1p36.33-p32 in CRC [25] // deletion of 13p36.3 in 25% of neuroblastomas and 87% of cell lines [45] // loss of expression and genomic deletion on 1p [17]

loss

1p36.13

1p36.11

PADI1

DKFZP434L0117

E2F2 // ID3 // loss of 1p36.1 in CRC [22, 25] // loss of expression and genomic deletion on 1p [17]

loss

1p35.1

1p34.3

HDAC1

PSMB2

LCK at 1p35.1 // hereditary CRC at 1p35 (OMIM 114500) // loss of expression and genomic deletion on 1p [17]

gain

1q32.1

1q41

PIGR

DKFZp547M236

1q32 amplification involving MDM4 and CNTN2 in malignant gliomas [46]

gain

2p25.3

2p24.2

Hs.8379.0

VSNL1

hereditary CRC at 2p25 (OMIM 114500)

loss

2p11.2

2q12.1

MAT2A

MGC11332

83% loss of 2p11 in mantle cell lymphoma [47] // loss in mantle cell lymphoma [48]

gain

2q31.3

2q32.2

SSFA2

NAB1

hereditary HNPCC3 at 22q31-q33 (OMIM 600258) // familial breast cancer at 2q (OMIM 114480)

gain

2q33.2

2q35

Hs.163603

AAMP

familial breast cancer at 2q (OMIM 114480)

loss

2q37.3

2q37.3

SCLY

FARP2

familial breast cancer at 2q (OMIM 114480)

gain

3p25.3

3p25.1

KIAA0121

CAPN7

amplification of 3p25.2 in CRC [25] // RAF1 at 3p25.2 // FBLN1 at 3p25.2

gain

3p25.1

3p24.2

RAFTLIN

THRB

 

gain

3p24.2

3p23

FLJ20604

CLASP2

 

loss

3p21.31

3p21.31

CELSR3

NPR2L

hereditary HNPCC2 at 3p21.3 (OMIM 609310) // RASFF1

gain

3p11.1

3q13.11

MGC26717

ALCAM

frequent 3q11.2-q13.1 amplifications in cervix carcinomas [49]

loss

3q13.13

3q21.2

Hs.23762.0

ITGB5

 

loss

4p15.32

4p14

LAP3

Hs.118993

deletions of 4p14 in CRC [24] // SLIT2 at 4p15 is inactivated by hypermethylation in gliomas [33] // SLIT2 suppresses tumor growth [32] // loss of expression and genomic deletion on 1p [17]

loss

4q13.2

4q13.3

YT521

CXCL6

global loss of expression and genomic deletion on 4 [17]

loss

4q21.21

4q22.3

PRKG2

LIM

transition of follicular B cell lymphoma to diffuse large cell lymphoma accompanied by 4q21-q23 deletions // global loss of expression and genomic deletion on 4 [17]

loss

4q34.1

4q35.2

HPGD

Hs.130535

deletion of 4q34-q35 in colorectal cancer cell lines [25] // CASP3 at 4q34.3 // global loss of expression and genomic deletion on 4 [17]

loss

5q15

5q23.2

Hs.444378

Hs.97104

hereditary colorectal adenoma and carcinoma 1 (CRAC1) (OMIM 601228) at 15q15.3-q221 // APC at 5q21 // loss of expression and genomic deletion on 5q [17]

gain

5q31.1

5q31.3

HTGN29

Hs.443121

loss of expression and genomic deletion on 5q [17]

loss

5q31.3

5q33.1

NDFIP1

FLJ10290

amplification of 5q32-q34 in prostate cancer [50] // PDGFRB at 5q32 // loss of expression and genomic deletion on 5q [17]

gain

5q33.2

5q35.1

MRPL22

FBXW1B

amplification of 5q32-q34 in prostate cancer [50] // loss of expression and genomic deletion on 5q [17]

gain

6p25.3

6p24.2

DUSP22

NEDD9

amplification of 6p25 in 24% of mantle cell lymphomas [47] // amplification of 6p25 in 75% of prostate cancers [51]

loss

6p22.3

6p22.2

CAP2

SLC17A4

most frequent amplification of 6p22.3 in bladder cancer arrayCGH study [52]

loss

6p21.32

6p21.32

PBX2

RAB2L

 

gain

6p21.31

6p21.2

HMGA1

RNF8

CDKN1A at 6p21.2 // PIM1 at 6p21.2

gain

6q23.3

6q24.2

DUFD1

Hs.12565

amplification of 6q23-q24 assosicated with short survival [22]

gain

7p22.3

7p21.3

FLJ23471

ICA1

hereditary HNPCC4 at 7p22 (gene PMS2) // gain of expression and genomic amplification of 7 [17]

gain

7p21.2

7p15.3

ETV1

OSBPL3

amplification of 7p21 in mantle cell lymphomas [47] // amplification of 7p21 in osteosarcoma [53] // gain of expression and genomic amplification of 7 [17]

gain

7p14.3

7p13

LSM5

NPC1L1

gain of expression and genomic amplification of 7 [17]

loss

7q11.23

7q21.3

SRCRB4D

CAS1

amplification of 7q11.1-q12 in metastatic CRC [24] // gain of expression and genomic amplification of 7 [17]

gain

7q31.31

7q33

FAM3C

MGC5242

prostate cancer aggressiveness linked to 7q32-q33 [54] // gain of expression and genomic amplification of 7 [17]

gain

8q11.23

8q21.11

ATP6V1H

ANKTM1

amplifications of 8q11-q24 in metastasing CRC [29] // LYN at 8q12.1 // MOS at 8q12.1 // familial breast cancer at 8q11 (OMIM 114480) // amplifications at 8q in CRC [18, 21, 23, 25] // gain of expression and genomic amplification of 8q [17]

gain

8q22.3

8q24.22

TIEG

SLA

amplifications of 8q11-q24 in metastasing CRC [29] // MYC at 8q24.21 // PVT1 at 8q24.21 // amplification of 8q23-q24 in prostate cancer [55]// gain of expression and genomic amplification of 8q [17]

loss

9p21.3

9p21.1

IFNA4

SMU-1

loss of 9p21 in CRC [25] // TUBE1 at 9p21 // CDKN2A alias p16INK4A at ??? // frequent deletion of 9p21 in prostate cancer [56] // deletion of 9p21.3 in bladder cancer [57]

loss

9p13.3

9p13.3

BAG1

OPRS1

frequent LOH at 9p13-p21 in melanoma [58]

loss

9q21.11

9q21.32

Hs.173519.0

Hs.522256

loss of 9q21-q22 in mantle cell lymphoma [59]

loss

9q34.11

9q34.11

FLJ14596

GPR107

ABL1 protooncogene at 9q34.12

loss

10p15.3

10p12.2

Hs.255096

Hs.57079.0

frequent LOH of 10p15 in gastric cancer [60] // telomerase repressor at 10q15.1 [61] // deletion of 10p14 in mantle cell lymphoma [47, 59] // OPTN at 10p14 [62]

loss

10q11.21

10q11.23

Hs.173866.0

MOB

RET at 10q11.21 // LOH in prostate cancer at 10q11.21 [51]

loss

11p15.5

11p15.5

RNH

MUC5AC

hereditary CRC at 11p15.5 / HRAS at 11p15.5 // 11p15.5 methylation-dependent expression silencing and imprinting in phaeochromocytomas [63]

gain

11p15.5

11p15.4

CTSD

SSA1

CTSD (Cathepsin D) at 11p15.5 // familial breast cancer at 11p15.5 (OMIM 114480)

gain

11p13

11p12

Hs.120054.0

TRAF6

WT1 at 11p13

gain

11p11.2

11q12.1

ch-TOG

CTNND1

 

loss

11q13.2

11q13.4

LOC338692

SKD3

BCL1 at 11q13.3 (anti-apoptotic, amplified in breast cancer) // CCND1 at 11q13.3 (amplified in breast cancer [64]) // FGF3 at 11q13

gain

11q14.1

11q21

Hs.26339.0

MTMR2

 

loss

11q23.3

11q23.3

AMICA

HYOU1

frequent loss of 11q23.3-q25 in neuroblastoma [65] // loss of 11q23 in 33% of 73 tumor types [66]

loss

12p13.31

12p13.2

TPI1

CLEC1

CDKN1B (alias p27Kip1) at 12p13.2

loss

12p12.3

12q12

CGI-26

MADP-1

familial breast cancer at 12p12.1 (OMIM 114480)

gain

12q14.2

12q22

Hs.132260.0

Hs.403150

MDM2 at 12q15 // validated up-regulation of GPR49 at 12q21.1

gain

12q22

12q23.3

USP44

KIAA1033

 

loss

12q23.3

12q24.11

SART3

Hs.18370.0

loss of 12q24 in pancreas tumors [55]

gain

13q14.11

13q22.1

LOC283508

PIBF1

RB1 at 13q14.2 // ARLT1 at 13q14 // gain of expression and genomic amplification of 13q [17]

gain

14q22.1

14q22.2

PSMC6

AND-1

14q22-q23 losses in 25% of tumor types [66]

loss

14q24.1

14q24.3

Hs.369329

Hs.169812

hereditary CRC at 14q24.3 (OMIM 114500) // loss of 14q24-31 in CRC metastases [36] // FOS at 14q24.3 // hereditary HNPCC7 at 14q24.3 (gene MLH3) (OMIM) // poor prognosis when 14q24-q31 is lost in renal cell carcinoma [67] // loss of expression and genomic DNA of 14q [17]

loss

14q32.33

14q32.33

ZFYVE21

Hs.248015.0

14q32 is a tumor suppressive region in esophagal cancer [68] // loss of expression and genomic DNA of 14q [17]

loss

15q21.1

15q22.31

FBN1

CLPX

association between loss of 15q21.1-q22.2 and survival in hepatocellular carcinoma [69] // allelic imbalance at 15q21.1 in breast cancer metastases [70] // loss of expression and genomic DNA of 15q [17]

loss

15q26.1

15q26.3

GABARAPL3

FLJ25222

loss of expression and genomic DNA of 15q [17]

loss

16p12.1

16p11.2

GTF3C1

PRSS8

 

loss

16q12.1

16q13

TRF4-2

FLJ13154

 

gain

16q22.1

16q22.2

PSMB10

KIAA0931

CDH1 (E-Cadherin) at 16q22.1

loss

17p13.3

17p13.2

RPA1

DHX33

loss of 17p13.2 in CRC [25] // DHX33 at 17p13.2

loss

17p13.1

17p11.2

GAS7

COPS3

Near TP53 at 17p13.1 .// hereditary CRC at 17p11.2 (OMIM 114500) // hereditary CRC at 17p13.1 (OMIM 114500) // // familial breast cancer at 17p13 (OMIM 114480) // loss of 17p12 in CRC [25] // ELAC2 at 17p11.2

gain

17q21.33

17q23.2

TOB1

PPM1D

NME1 (NME23) at 17q21.33 // familial breast cancer at 17q22-q23 (OMIM 114480) //

loss

18p11.21

18q12.1

MGC24180

DSC3

loss of expression and genomic DNA of 18 [17]

loss

18q21.1

18q23

CGBP

MBP

DCC at 18q21.3 (OMIM 120470) // loss of 18q21.1 in CRC cell lines [25] // SMAD2 // SMAD4 mutations in CRC [71] // loss of expression and genomic DNA of 18 [17]

loss

19p13.3

19p13.3

DF

APCL

 

gain

19p13.2

19p13.12

FLJ20244

NOTCH3

 

gain

19p13.11

19q13.12

LOC114977

TYROBP

NIFIE14 at 19q13.12

loss

19q13.2

19q13.32

MGC20255

TOMM40

AKT2 (breast carcinoma at 19q13.2 // TGFB1 at 19q13.2 // proapototic Bax at 19q13.33

gain

20p11.21

20q11.21

C1QR1

BCL2L1

 

gain

20q11.22

20q11.23

RNPC2

C20orf102

SRC at 20q11.23 (overexpressed in breast carcinoma) // gain of expression and genomic DNA of 20q [17]

gain

20q13.12

20q13.33

SLC12A5

ARFRP1

gain of expression and genomic DNA of 20q [17]

gain

21q22.12

21q22.3

C21orf18

TMPRSS2

ETS2 at 21q22.2

loss

21q22.3

21q22.3

PFKL

COL6A1

COL18A1 (Endostatin) at 21q22.3

loss

22q11.21

22q12.1

SDF2L1

TPST2

familial breast cancer at 22q12.1 (OMIM 114480)

loss

22q13.31

22q13.33

Hs.296370.0

RABL2B

hereditary CRC at 22q13 (OMIM 114500)

gain

Xp22.13

Xp22.11

SCML1

ARX

 

gain

Xp11.22

Xp11.1

Hs.3383.1

Hs.224455

 

gain

Xq24

Xq26.3

FLJ32122

CXX1

 
  1. These are condensed results of the ChARM analyses: overlapping regions with evidence for up- or down-regulation from various analyses of different cross-correlation window sizes have been fused into single regions. The original ChARM output including p values for each region and additional annotation can be found in Additional file 1. Hereditary colorectal cancer syndromes are indicated along with their OMIM ID. Gene symbols are official or provisional HUGO symbols if available, otherwise names of Unigene clusters. Information about known tumor genes in misregulated regions were extracted from the literature. Tumor-associated genes are located within expression islands or in near vicinity.